Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (11)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Fillion, J.
Right arrow Articles by Bellon, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fillion, J.
Right arrow Articles by Bellon, B.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol 9, 263-271, Copyright © 1997 by Oxford University Press


ARTICLES

Evidence for heterogeneous TCR V beta repertoire expression in mercury- induced immune disorders in rats

J Fillion, R Baccala, C Pannetier, J Kuhn, P Druet and B Bellon
INSERM U430, Hopital Broussais, Paris, France.

Administration of subtoxic doses of HgCl2 affects differentially the immune system depending on the strain of rats tested. Susceptible Brown- Norway (BN) rats exhibit a CD4+ T cell-dependent polyclonal activation of B cells; in contrast, Lewis (LEW) rats are resistant and develop an immunosuppression mediated by CD8+ T cells recruited by CD4+ T cells. The mechanisms by which mercury induces immune disorders are poorly understood. We were interested in analyzing the diversity and mercury- mediated changes of the TCR Vbeta repertoire in the BN and LEW strains of rats at different times of HgCl2 exposure. Our results obtained after analysis of lymph node T cells by RNase protection assay, flow cytometry or immunoscope assay (i) were not consistent with a superantigen-like stimulus since we observed neither a V beta-selective expansion nor deletion that would have been expected and (ii) showed that in BN rats, as well as in LEW rats, an increase in the number of T cells was associated with the heterogeneous TCR V beta repertoire, thus supporting a polyclonal T cell activation. However, in BN rats the total number of T cells increased very rapidly, whereas in LEW rats only CD8+ T cells accumulated.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Immunol.Home page
M. Guillet, S. Brouard, K. Gagne, F. Sebille, M.-C. Cuturi, M.-A. Delsuc, and J.-P. Soulillou
Different Qualitative and Quantitative Regulation of V{beta} TCR Transcripts During Early Acute Allograft Rejection and Tolerance Induction
J. Immunol., May 15, 2002; 168(10): 5088 - 5095.
[Abstract] [Full Text] [PDF]


Home page
Int ImmunolHome page
A.-C. Field, L. Caccavelli, J. Fillion, J. Kuhn, C. Mandet, P. Druet, and B. Bellon
Neonatal induction of tolerance to Th2-mediated autoimmunity in rats
Int. Immunol., October 1, 2000; 12(10): 1467 - 1477.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
A. Badou, M. Savignac, M. Moreau, C. Leclerc, R. Pasquier, P. Druet, and L. Pelletier
HgCl2-induced Interleukin-4 Gene Expression in T Cells Involves a Protein Kinase C-dependent Calcium Influx through L-type Calcium Channels
J. Biol. Chem., December 19, 1997; 272(51): 32411 - 32418.
[Abstract] [Full Text] [PDF]


Home page
JEMHome page
F. Bridoux, A. Badou, A. Saoudi, I. Bernard, E. Druet, R. Pasquier, P. Druet, and L. Pelletier
Transforming Growth Factor {beta} (TGF-{beta})-dependent Inhibition of T Helper Cell 2 (Th2)-induced Autoimmunity by Self-Major Histocompatibility Complex (MHC) Class II-specific, Regulatory CD4+ T Cell Lines
J. Exp. Med., May 19, 1997; 185(10): 1769 - 1775.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.